The protective effects of DL-Selenomethionine against T-2/HT-2 toxins-induced cytotoxicity and oxidative stress in broiler hepatocytes. (February 2019)

• Record Type: Journal Article
• Authors: Yang, Lingchen; Tu, Di; Wang, Naidong; Deng, Zhibang; Zhan, Yang; Liu, Wei; Hu, Yi; Liu, Tanbin; Tan, Lei; Li, Yalan; Guo, Shiyin; Wang, Aibing
• Is Part Of: Toxicology in vitro. Volume 54(2019)
• Page Start: 137
• Page End: 146
• Publication Date: 2019-02
• Subjects: T-2/HT-2 toxins -- Hepatocytes -- Cytotoxicity -- Oxidative stress -- DL-Selenomethionine -- Protective effects; T-2 T-2 toxin -- HT-2 HT-2 toxin -- LDH Lacate dehydrogenase -- ROS release, reactive oxygen species -- MDA malondialdehyde -- GSH glutathione -- SOD superoxide dismutase -- CAT catalase -- GSH-PX glutathione peroxidase -- NAC N-Acetyl-cysteine -- Se Selenium -- DMEM Dulbecco's modified Eagle's medium -- FCS fetal calf serum -- MTT thiazolyl blue tetrazolium bromide -- DCFH-DA 2′, 7′-Dichlorofluorescein diacetate -- GST Glutathione S-transferase; Toxicity testing -- In vitro -- Periodicals; Toxicology -- Periodicals; 615.9
• DOI: 10.1016/j.tiv.2018.09.016
• Languages: English
• ISSNs: 0887-2333

Abstract

Abstract: T-2 and HT-2 toxins can cause cytotoxicity and oxidative stress in animals, while DL-Selenomethionine plays an important role in preventing oxidative stress and improving cell viability. However, the role of DL-Selenomethionine in T-2/HT-2 toxins-induced cell damage is still unknown. In this study, we investigated whether DL-Selenomethionine plays a protective role against T-2/HT-2-induced cytotoxicity and oxidative stress in primary hepatocytes. Our results demonstrated that T-2/HT-2 toxins-exposed broiler hepatocytes exhibited significantly decreased cell viability and intracellular glutathione (GSH) concentration while increased Lacate dehydrogenase (LDH) leakage, intracellular reactive oxygen species (ROS), glutathione peroxidase (GSH-PX), malondialdehyde (MDA) and catalase (CAT) levels, as well as elevated expression levels of genes related to oxidative stress, in a toxin dose-dependent manner ( P < 0.05). However, the application of DL-Selenomethionine into T-2/HT-2 treated hepatocytes effectively alleviated the adverse effects of T-2/HT-2, as demonstrated by increased cell viability, decreased LDH leakage, declined intracellular ROS and MDA levels, increased expression of oxidative stress-related genes, as well as accordingly enhanced activities of GSH, GSH-PX, SOD and CAT as compared to the control groups ( P < 0.05). Therefore, our in vitro data demonstrate that DL-Selenomethionine can function as an effectively protective agent against T-2/HT-2-induced cytotoxicity and oxidative stress. Highlights: DL-Selenomethionine preserved the viability of hepatocytes exposed to T2/HT2 challenge. T2/HT2 toxins-induced oxidative stress could be inhibited by DL-Selenomethionine. DL-Selenomethionine regulated the expression and activities of major antioxidases.